Difference between revisions of "Part:BBa K364307:Experience"
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In the absence of hormone, estrogen receptors are largely located in the cytosol. Hormone binding to the receptor triggers a number of events starting with migration of the receptor from the cytosol into the nucleus, dimerization of the receptor, and subsequent binding of the receptor dimer to specific sequences of DNA. Some of the effects in humans: Createing proliferative endometrium,breast cell stimulation, increased body fat and weight gain, salt and fluid retention, increased risk of blood clots. | In the absence of hormone, estrogen receptors are largely located in the cytosol. Hormone binding to the receptor triggers a number of events starting with migration of the receptor from the cytosol into the nucleus, dimerization of the receptor, and subsequent binding of the receptor dimer to specific sequences of DNA. Some of the effects in humans: Createing proliferative endometrium,breast cell stimulation, increased body fat and weight gain, salt and fluid retention, increased risk of blood clots. | ||
| − | + | ===Applications of BBa_K364307=== | |
| − | + | This part can be fused with different LBDs to get a composite nuclear receptor binging to the chosen DBD's binding site and activating gene expression. | |
===References=== | ===References=== | ||
Revision as of 21:48, 24 October 2010
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Physiological functions
In the absence of hormone, estrogen receptors are largely located in the cytosol. Hormone binding to the receptor triggers a number of events starting with migration of the receptor from the cytosol into the nucleus, dimerization of the receptor, and subsequent binding of the receptor dimer to specific sequences of DNA. Some of the effects in humans: Createing proliferative endometrium,breast cell stimulation, increased body fat and weight gain, salt and fluid retention, increased risk of blood clots.
Applications of BBa_K364307
This part can be fused with different LBDs to get a composite nuclear receptor binging to the chosen DBD's binding site and activating gene expression.
References
Dahlman-Wright K, Cavailles V, Fuqua SA, Jordan VC, Katzenellenbogen JA, Korach KS, Maggi A, Muramatsu M, Parker MG, Gustafsson JA (2006). "International Union of Pharmacology. LXIV. Estrogen receptors". Pharmacol. Rev. 58 (4): 773–81. doi:10.1124/pr.58.4.8.
Levin ER (2005). "Integration of the extranuclear and nuclear actions of estrogen". Mol. Endocrinol. 19 (8): 1951–9. doi:10.1210/me.2004-0390.
Leung YK, Mak P, Hassan S, Ho SM (August 2006). "Estrogen receptor (ER)-beta isoforms: a key to understanding ER-beta signaling". Proc Natl Acad Sci USA 103 (35): 13162–7.
Deroo BJ, Korach KS (2006). "Estrogen receptors and human disease". J. Clin. Invest. 116 (3): 561–7.
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